Thin-capped fibroatheroma (“TFCA”) or vulnerable plaque refers to an atherosclerotic plaque that may develop inside a blood vessel, such as an artery. The typical vulnerable plaque contains a core filled with lipids, cholesterol crystals and cholesterol esters, macrophages, and other cells. The core has a thin fibrous cap (0.05 millimeters (mm) to 0.10 mm thickness). The fibrous cap may become weakened and rupture. When ruptured, the luminal blood becomes exposed to highly thrombogenic material from the core of the vulnerable plaque, which can result in total thrombotic occlusion of the blood vessel.
There is increasing evidence that the propensity of a vulnerable plaque to rupture is related to an activity of matrix metalloproteinases (“MMPs”), largely synthesized by macrophage-derived foam cells. Specifically, MMPs may degrade extracellular matrix proteins, such as Types I and III collagen that are a significant source of fibrous cap structural integrity. Thus, chronic and/or local inflammation, typically a result of monoctye adhesion, in the plaque can lead to destabilization of the vulnerable plaque and acute coronary syndromes (via thrombosis).
Researchers believe that vulnerable plaque is formed in the following way. Fat droplets are absorbed by the blood vessel (e.g., artery), which causes the release of cytokines (proteins) that lead to inflammation. The cytokines make the artery wall sticky, which attracts monocytes (immune system cells). The monocytes squeeze into the artery wall. Once inside, the monocytes turn into macrophages (cells) and begin to soak-up fat droplets. The fat-filled macrophages form a plaque with a thin covering.
Improvements in imaging techniques, such as optical coherence tomography (“OCT”) and intravascular ultrasound (“IVUS”) offer the opportunity to identify a vulnerable plaque. A need exists, however, for effective methods to treat (e.g., remove, immobilize, reshape) a vulnerable plaque.